| 引用本文:庞春红，李澎涛，朱晓磊.脑缺血-再灌注相关细胞因子表达的TNF-α损伤机制及清开灵的作用[J].世界中医药,2011,6(4):. |
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| 脑缺血-再灌注相关细胞因子表达的TNF-α损伤机制及清开灵的作用 |
| Impairment Mechanism of TNF-α in Ischemia-reperfusion Rats and Effect of Qingkailing |
| 投稿时间：2011-05-12 |
| DOI： |
| 中文关键词: 缺血-再灌注 TNF-α TNF-α抗体 清开灵 |
| English Keywords:Ischemia reperfusion TNF-α TNF-αantibody Qingkailing |
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| 中文摘要: |
| 目的：探讨缺血-再灌注大鼠相关细胞因子的TNF-α损伤机制以及清开灵的作用特征。方法：健康雄性Wistar大鼠，利用双侧颈总动脉夹闭的方法复制大鼠前脑缺血-再灌注模型，分别给予清开灵注射液、TNF-α抗体及该抗体与清开灵共用。选择再灌注24h和72h两个时间点，检测血清TNF-α、血清可溶性细胞间黏附分子-1(sICAM-1)、血清P-选择素(P-selectin)含量以及脑组织细胞间黏附分子-1(ICAM-1)表达量。结果：清开灵具有降低升高的血清TNF-α含量的趋势，而TNF-α抗体的作用随时间延长而增强；清开灵和TNF-α抗体均能够有效地降低外周血sICAM-1水平、脑组织ICAM-1含量和血清P-selectin含量，阻断TNF-α后更明显，而且使清开灵的作用更为显著。结论：脑缺血-再灌注导致的损伤与微血管内外炎性细胞因子的毒性损害有密切关系，并与黏附分子导致血中白细胞与内皮细胞的黏附有关。 |
| English Summary: |
| To investigate impairment mechanism of TNF-α in ischemia-reperfusion rats and effect of Qingkailing. Methods:The ischemia-reperfusion model of rats was established by performing double common carotid clamping on adult male Wistar rats. Qingkailing, antibody-TNF-α, Qingkailing +anti-TNF-α were receptively administered to the model. We observed serum TNF-α、serum sICAM-1、serum p-selectin and expression of brain tissue ICAM-1 at 24h and 72h. Results:A tendency was observed in Qingkailing to reduce the increasing level of serum TNF-α, which intensified over time. Qingkailing and antibody-TNF-α can reduce expression of peripheral blood sICAM-1、P-selectin, and brain tissue ICAM-1. The effect was more obvious after blocking TNF-α, and the effect of Qingkailing was more significant. Conclusion: The BBB injury due to cerebral ischemia-reperfusion is related closely to the toxicity of inflammary cytokine inside and outside the blood capillary, and also related to the adherence between white blood cells and endothelial cells caused by adhesion molecule. |
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